microRNA-126 抑制人牙髓细胞中的血管细胞黏附分子-1 和白细胞介素-1β。
microRNA-126 inhibits vascular cell adhesion molecule-1 and interleukin-1beta in human dental pulp cells.
机构信息
Department of General Dentistry, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, College of Stomatology, Shanghai Jiao Tong University, National Center for Stomatology, National Clinical Research Center for Oral Diseases, Shanghai Key Laboratory of Stomatology, Shanghai, China.
Iowa Institute for Oral Health Research, College of Dentistry, The University of Iowa, Iowa City, Iowa, USA.
出版信息
J Clin Lab Anal. 2022 May;36(5):e24371. doi: 10.1002/jcla.24371. Epub 2022 Mar 25.
BACKGROUND
Vascular cell adhesion molecule (VCAM-1) mediates pulpitis via regulating interleukin (IL)-1β. microRNA (miR)-126 was reported to regulate the VCAM-1 under many different pathophysiological circumstances. We investigated variations of miR-126 and VCAM-1 in inflamed patient pulp tissues and determined potential roles of miR-126 in pulpitis using human dental pulp cells (hDPCs) in vitro.
METHODS
We quantitatively measured the transcripts of miR-126 and VCAM-1 in inflamed human pulp tissues using qRT-PCR and compared with those from healthy human pulp tissues. In addition, we transfected miR-126 in hDPCs using plasmid DNA (pDNA)-encoding miR-126 delivered by polyethylenimine (PEI) nanoparticles.
RESULTS
The irreversible pulpitis significantly reduced miR-126 and increased the transcript of VCAM-1 in pulp tissues (p < 0.05). pDNA-encoding miR-126 delivered PEI nanoparticles and effectively upregulated the expression of miR-126 in hDPCs (p < 0.05). The overexpression of miR-126 could effectively suppress the transcripts and protein levels of VCAM-1 and IL-1β induced by Pg-LPS at 100ng/mL in DPCs (p < 0.05).
CONCLUSIONS
miR-126 is involved in pulpitis and downregulated the VCAM-1 and IL-1β in DPCs. miR-126 may be a potential target to attenuate the inflammation of pulpitis.
背景
血管细胞黏附分子 (VCAM-1) 通过调节白细胞介素 (IL)-1β 介导牙髓炎。有报道称，microRNA (miR)-126 在许多不同的病理生理情况下调节 VCAM-1。我们研究了炎症患者牙髓组织中 miR-126 和 VCAM-1 的变化，并通过体外人牙髓细胞 (hDPC) 确定 miR-126 在牙髓炎中的潜在作用。
方法
我们使用 qRT-PCR 定量测量了炎症人牙髓组织中 miR-126 和 VCAM-1 的转录物，并与健康人牙髓组织进行了比较。此外，我们使用聚乙烯亚胺 (PEI) 纳米颗粒递送的质粒 DNA (pDNA) 编码 miR-126 转染 hDPC。
结果
不可逆性牙髓炎显著降低了牙髓组织中的 miR-126，并增加了 VCAM-1 的转录物（p<0.05）。pDNA 编码的 miR-126 通过 PEI 纳米颗粒传递，并有效地上调了 hDPC 中 miR-126 的表达（p<0.05）。miR-126 的过表达可有效抑制 Pg-LPS 在 100ng/mL 诱导的 hDPC 中 VCAM-1 和 IL-1β 的转录物和蛋白水平（p<0.05）。
结论
miR-126 参与牙髓炎，下调 DPCs 中的 VCAM-1 和 IL-1β。miR-126 可能是减轻牙髓炎炎症的潜在靶点。
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